ArticleOncogene2006
Evi1 is a survival factor which conveys resistance to both TGFbeta- and taxol-mediated cell death via PI3K/AKT.
Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
What it found
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Who cites it
43 citing papers in PubMed, 103 citations in OpenAlex.
- High EVI1 and PARP1 expression as favourable prognostic markers in high-grade serous ovarian carcinoma.Journal of ovarian research · 2023Article
- AKT inhibition sensitizes EVI1 expressing colon cancer cells to irinotecan therapy by regulating the Akt/mTOR axis.Cellular oncology (Dordrecht, Netherlands) · 2022Article
- Article
- EVI1 in Leukemia and Solid Tumors.Cancers · 2020Review
- Article
- MiR-30a regulates cancer cell response to chemotherapy through SNAI1/IRS1/AKT pathway.Cell death & disease · 2019Article
- Chemotherapy Resistance in Advanced Ovarian Cancer Patients.Biomarkers in cancer · 2019Review
- EVI1 carboxy-terminal phosphorylation is ATM-mediated and sustains transcriptional modulation and self-renewal via enhanced CtBP1 association.Nucleic acids research · 2018Article
- Ecotropic viral integration site 1 promotes metastasis independent of epithelial mesenchymal transition in colon cancer cells.Cell death & disease · 2018Article
- Insights into the role of reactive sulfhydryl groups of Carbonic Anhydrase III and VII during oxidative damage.Journal of enzyme inhibition and medicinal chemistry · 2017Review
- Article
- Intratumoral Heterogeneity of Frameshift Mutations in MECOM Gene is Frequent in Colorectal Cancers with High Microsatellite Instability.Pathology oncology research : POR · 2017Article
- Evi1 regulates Notch activation to induce zebrafish hematopoietic stem cell emergence.The EMBO journal · 2016Article
- CSTB Downregulation Promotes Cell Proliferation and Migration and Suppresses Apoptosis in Gastric Cancer SGC-7901 Cell Line.Oncology research · 2016Article
- Mutations in MECOM, Encoding Oncoprotein EVI1, Cause Radioulnar Synostosis with Amegakaryocytic Thrombocytopenia.American journal of human genetics · 2015Article
- EVI1, a target gene for amplification at 3q26, antagonizes transforming growth factor-β-mediated growth inhibition in hepatocellular carcinoma.Cancer science · 2015Article
- EVI1 promotes tumor growth via transcriptional repression of MS4A3.Journal of hematology & oncology · 2015Article
- Correlations of common polymorphism of EVI-1 gene targeted by miRNA-206/133b with the pathogenesis of breast cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Article
- EVI1 oncogene promotes KRAS pathway through suppression of microRNA-96 in pancreatic carcinogenesis.Oncogene · 2014Article
- EVI1 expression in childhood acute lymphoblastic leukaemia is not restricted to MLL and BCR/ABL rearrangements and is influenced by age.Blood cancer journal · 2014Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
In hematopoietic cells the transforming potential of the ecotropic viral integration site 1 (Evi1) oncogene is thought to be dependent upon the ability to inhibit TGFbeta signaling. Although Evi1 has recently been implicated in certain epithelial cancers, the effects of Evi1 on transformation and TGFbeta signaling in epithelial cells are not completely understood. Herein, we have determined the effects of Evi1 on TGFbeta signaling in intestinal epithelial cells. Stable expression of Evi1 in non-transformed intestinal epithelial cells inhibited induction of some Smad3-dependent TGFbeta target genes, such as PAI1. However, TGFbeta-mediated induction of cellular adhesion signaling components such as integrin1 and paxillin was not inhibited by Evi1; nor did Evi1 inhibit TGFbeta-mediated epithelial to mesenchymal transition. Likewise, Evi1 did not inhibit TGFbeta-mediated downregulation of cyclin D1 or block TGFbeta-mediated growth inhibition. However, Evi1 did inhibit TGFbeta-mediated apoptosis by a process that involves phosphoinositide-3-kinase (PI3K) and its downstream effector AKT. The ability of Evi1 to suppress apoptosis is not restricted to TGFbeta-mediated cell death, since Evi1 also protects intestinal epithelial cells from taxol-mediated apoptosis. Evi1 is overexpressed in some human colon cancer cell lines, and overexpression is associated with amplification of the Evi1 gene. Knockdown of Evi1 by siRNA inhibited AKT phosphorylation in HT-29 human colon cancer cells and increased their sensitivity to taxol-mediated apoptosis. These data indicate that Evi1 functions as a survival gene in intestinal epithelial cells and colon cancer cells, activating PI3K/AKT and conveying resistance to both physiological and therapeutic apoptotic stimuli.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.